Diabetes mellitus is a multisystemic chronic disease in which all types of metabolism are disrupted.It is characterized by impairment of insulin secretion or function, accumulation of glucose in the blood (hyperglycemia), urine (glucosuria) and the development of complications.
Endocrinologists with several years of experience in the field of endocrinology work at the modern clinic.Doctors will be able to correctly determine the degree of compensation of diabetes mellitus, identify existing complications and prescribe or modify the treatment program.
How does glucose metabolism usually take place?
Glucose is the body's main source of energy.It enters the body with food, mainly carbohydrates, or it is synthesized from fats and proteins during a series of metabolic reactions.Excess glucose accumulates in the liver and muscles in the form of glycogen and is used as needed.
All tissues of the human body are divided into insulin-dependent (muscles, adipose tissue, heart muscle cells) and non-insulin-dependent (brain, red blood cells, cornea, liver, kidneys) parts.In order for glucose to enter the cells of insulin-dependent tissue and be used in cellular metabolism, insulin is needed.It is produced in the β cells of the pancreas.Insulin acts as a key that opens the lock for glucose to enter the cell.Insulin-independent tissues receive glucose passively by simple diffusion.
When everything in the body is working properly, the process of glucose reaching insulin-dependent tissues takes place dynamically and no problems arise.If insulin production is interrupted (for example, if the pancreas is damaged) or its mechanism of action on the cell is interrupted (the cell barrier is interrupted), glucose accumulates in the body and the cells starve.
Below we look at what happens when glucose builds up in the body and look at the different types of diabetes.
Classification
Experts distinguish several main types of diabetes.We focus on the four most common:
- Type I (old name: insulin dependent);
- II.type (old name: non-insulin dependent);
- Pregnancy;
- Symptomatic.
Let's look at each type in more detail.
Type I diabetes mellitus
This type of diabetes mellitus develops as a result of damage to the β-cells of the pancreas, the body's source of insulin, which results in a state of absolute insulin deficiency.One of the common causes of cell damage is the development of an autoimmune process, when the body begins to perceive the cells of the pancreas as foreign.Antibodies accumulate against them, which completely destroy the source of insulin.
Other causes of pancreatic beta cell death:
- effects of chemicals (nitrosamine, pesticides, some drugs);
- infectious disease (measles, rubella viruses, cytomegalovirus);
The disease develops when more than 80% of the cells die.
Type I diabetes mellitus is characteristic of young people and often begins at an early age, in an acute form, with a rapid increase in clinical symptoms.
Type II diabetes mellitus
Type II diabetes mellitus (formerly known as: non-insulin dependent) develops as a result of a violation of the cell's receptor apparatus, which results in the development of insulin resistance in the body.
In this type of diabetes mellitus, insulin is produced in the required amount, but the insulin-dependent cells do not respond to it.Relative insulin deficiency leads to reduced glucose utilization by muscle and adipose tissue, which contributes to the development of hyperglycemia.
Causes of type II diabetes include:
- hereditary predisposition;
- overnutrition, obesity;
- physical inactivity;
- chronic stress state.
Table 1. I. and II.comparative characteristics of type 2 diabetes mellitus.
| Sign |
Type I |
II |
| Prevalence |
15% |
85% |
| The beginning of the disease |
Most often in childhood or adolescence |
Middle and old age |
| Acute |
Long term progressive |
|
| Development of symptoms |
Fast |
Slow |
| Phenotype (appearance) |
Thin |
Obesity |
| Insulin level |
I miss you |
Enhanced |
| Insulin resistance |
- |
+ |
| Insulin deficiency |
Absolute |
Relative |
| Ketoacidosis |
+ |
- |
Gestational diabetes (diabetes during pregnancy)
Physiological pregnancy is characterized by two significant changes in glucose metabolism:
- Continuous supply of glucose to the placenta and fetus.During pregnancy, due to increased glucose consumption, its level in the body decreases faster than in a non-pregnant woman.
- A decrease in tissue insulin sensitivity in the second trimester of pregnancy, which results in the development of insulin resistance.
This condition is caused by an excess of hormones: progesterone, cortisol, prolactin, which have an anti-islet effect (block the effect of insulin).This reduces the insulin sensitivity of fat and muscle tissue.
Physiological pregnancy is characterized by both insulin resistance and a compensatory increase in pancreatic β-cell function, which helps maintain optimal glucose metabolism.In women with impaired glucose tolerance, the compensatory abilities of β-cells are insufficient, leading to the development of hyperglycemia.
Diagnosis of gestational diabetes mellitus
In order to reduce the risk of complications for the mother and the fetus, it is necessary to correctly diagnose and correct gestational diabetes mellitus.
The diagnosis is carried out in 2 stages:
- The first phase is performed when a pregnant woman consults a doctor for the first time before the 24th week of pregnancy.A woman undergoes one of the tests: venous blood is given on an empty stomach, a glucose tolerance test or glycated hemoglobin HbA1c is determined.
- The second phase is carried out in pregnant women who have not been identified in the early stages of carbohydrate metabolism disorders.Diabetes is diagnosed with a glucose tolerance test with 75 g of glucose between the 24th and 28th week of pregnancy.
A terhes nők éhomi glükóz normája kevesebb, mint 5,1 mmol/l. Egy óra elteltével az orális glükóz tolerancia teszt során a normatív értékek <10,0 mmol/l, 2 óra elteltével több mint 7,8 mmol/l és kevesebb, mint 8,5 mmol/l.
Abnormal indicators of venous blood sugar are the following values:
- more than 7.0 mmol/l on an empty stomach;
- glycated hemoglobin (HbA1) more than 6.5%;
- glucose value is more than 11.1 mmol/l (the time of day and the last meal do not count).
These cases indicate the manifestation of gestational diabetes mellitus and require immediate insulin treatment.
Elevated fasting values that do not meet the parameters of diabetes - more than 5.1 mmol / l, but less than 7.0 mmol / l - put a pregnant woman in the group exposed to an increased risk of diabetes.Such women are advised to follow a rational diet, dynamically control the glycemic level and the condition of the fetus.
Symptomatic diabetes mellitus
This type is secondary and is caused by impaired glucose metabolism due to various diseases or medications.These conditions are as follows:
- diseases of the exocrine pancreas (pancreatitis, cancer, cystic fibrosis);
- medicinal diabetes mellitus - when taking glucocorticosteroids (they have an anti-islet effect, reduce insulin production in the body), phenytoin, estrogens (oral contraceptives).
Symptomatic diabetes mellitus can usually be treated by treating the underlying cause of the diabetes (such as changing or stopping a medication).
Why is hyperglycemia bad?
We have already realized that the lack or dysfunction of insulin leads to the accumulation of glucose in the blood.When the renal threshold is reached (>8.8 mmol/l - the value at which the kidneys begin to transfer glucose when filtering the blood), glycosuria develops.Glucose is an osmotically active substance, therefore it binds water and leads to polyuria, a large loss of body water and compensatory activation of the thirst center.
Polyuria (excretion of large amounts of urine in large doses) leads to dehydration of the body, a decrease in the amount of blood in the bloodstream, a decrease in blood pressure, and hypoxia of peripheral tissues.This is fraught with the risk of thromboembolism and the development of disseminated intravascular coagulation syndrome.
In addition, the pressure drop is less than 50 mm.rt.Art.it leads to the slowing down of kidney blood flow, even to anuria (lack of urination) and the development of acute kidney failure.
There is a peculiarity in the pathogenesis of type I diabetes mellitus - the absolute lack of insulin leads to the activation of counterinsular hormones (insulin antagonists): T4, adrenaline, cortisol, somatotropic hormone, glucagon.
The following hormones increase all types of metabolism, leading to an even greater increase in glucose:
Lipolysis is the destruction of fats, which leads to the formation of large amounts of free fatty acids (FFA) and from them glucose.
FFA is an alternative source of energy in the body, which is the basis for the formation of ketone bodies (such as acetone).Elevation of ketones in the blood and urine causes vomiting, metabolic acidosis (decrease in blood pH) and compensatory hyperventilation of the lungs (noisy, deep acidotic Kussmaul breathing occurs).The accumulation of ketones leads to one of the serious complications - ketoacidotic coma.
- Gluconeogenesis is a metabolic pathway through which glucose is synthesized from non-carbohydrate sources (amino acids, fatty acids).
- Glycogenolysis is the process of breaking down glycogen (glucose storage in the liver).
Symptoms
We have dealt with the main correlations of the pathogenesis of diabetes mellitus, now we outline the clinical symptoms on the basis of which this disease can be suspected:
- thirst (polydipsia) - associated with dehydration of the body;
- frequent urination (polyuria) - due to the fact that glucose is osmotically active and binds water;
- increased appetite - due to the fact that glucose does not enter the cells, a state of energy starvation develops in them;
- dry skin, peeling, itching - these symptoms appear as a result of dehydration and dysfunction of the sweat and sebaceous glands;
- pustular skin diseases - occur as a result of a decrease in the body's resistance;
- weakness, depressed mood.
Early complications
Early complications are acute conditions characterized by a rapid increase in clinical symptoms and require immediate medical intervention from a physician.
Early complications of type I diabetes
- Ketoacidotic coma is more often observed in type 1 diabetes mellitus.It is characterized by a sharp, "fruity" odor from the mouth, confusion, impaired reflexes, diarrhea, nausea, and ketoacidotic Kussmaul respiration.
Other complications include loss of consciousness, reflexes and a drop in blood pressure:
- Hyperosmolar coma
- Lactic acidotic coma
- Hypoglycemic coma
Differential diagnosis of the type of coma is carried out by biochemical analysis of blood, urine and blood acid-base status.
Early complications of type II diabetes
- Hyperosmolar coma - observed more often
- Lactic acidotic coma
- Hypoglycemic coma
Late complications
These are:
- microangiopathies: retinopathy, nephropathy;
- macroangiopathies: coronary heart disease, angina pectoris, atherosclerosis, high blood pressure, chronic cerebral ischemia, acute cerebrovascular accident;
- neuropathies (polyradiculoneuropathy, radiculopathy, lumbar plexopathy);
- deposition of sorbitol in tissues (cataract);
- immune deficiencies: pustular diseases, prolonged tissue healing);
- diabetic foot - pathological changes in the peripheral nervous system, in the arterial and microcirculatory beds, in the osteoarticular apparatus of the foot, with the development of ulcerative-necrotic processes and gangrene.
Mechanisms of development of late complications
Late complications of diabetes are primarily associated with damage to blood vessels.Their main mechanism is the glycosylation of all protein structures of the body (vascular endothelium, basal membrane, blood vessels of nerve endings).
Glycosylated proteins:
- increases the permeability of the vessel wall and disrupts the rheological properties of blood, which causes thrombosis;
- promotes the production of pro-inflammatory factors that damage small capillaries;
- blocks vasodilation;
- increases lipid peroxidation, which results in the production of tissue-damaging reactive oxygen species;
- they contribute to the development of endothelial dysfunction and increase the risk of atherosclerosis.
As a result of these processes, the wall of the small blood vessels becomes stiff, inflexible and prone to rupture.In the small vessels, the speed of blood flow slows down and the viscosity of the blood increases.
Gray cataract
Cataracts are a common late complication of diabetes mellitus.
This is due to the fact that excess glucose enters alternative metabolic pathways.One of these pathways is the oxidation of the polyol sorbitol.Sorbitol is a compound that increases the osmotic pressure in the chambers of the eye and causes clouding of the lens.
Diabetic glomerulosclerosis
This nephropathy is accompanied by morphological changes in the capillaries and arterioles of the kidney glomeruli, which lead to their closure (blockage), sclerotic changes, a gradual decrease in the filtration function of the kidneys, and the development of chronic kidney failure.
Diabetic neuropathy and retinopathy
Diabetic neuropathy is characterized by damage to the central and peripheral nervous system, which is clinically manifested by a loss of sensitivity.
Diabetic retinopathy is characterized by damage to retinal capillaries, arterioles and venules with the appearance of microaneurysms, haemorrhages, exudative changes and newly formed blood vessels.
Treatment of diabetes
Type 1 diabetes mellitus is treated with insulin.Based on the duration of action of insulin, it is divided into:
- ultra-short-acting - used before every meal.The onset of the effect is 5-15 minutes, the duration is 2-5 hours;
- short-acting - used before every meal.It begins to work after 30 minutes and lasts for 5-8 hours;
- medium duration of action - starts working after 1-2 hours, duration of action 18-24 hours.It is necessary for the occurrence of basic energetic processes;
- long-acting - starts working after 1-2 hours, lasts 18-36 hours.It is necessary for basic energetic processes to occur.
Doctors treat type II diabetes mellitus in 3 stages.
The first stage of treatment:
- in persons of normal body weight - dietary therapy (restriction of foods rich in carbohydrates);
- Obesity therapy is carried out in overweight people: more active diet therapy (strict restriction of the total calorie content of food, carbohydrates and animal fats), regularly dosed (therapeutic) physical activity, lifestyle change, which means increasing physical activity at home and in leisure time.
The second stage of treatment:
- Use of β-cell stimulating drugs: sulfonylurea derivatives, biguanides;
- the use of drugs that increase the sensitivity of insulin receptors in muscle and fat tissue: thiazolidinediones.
Stage 3 of treatment: insulin therapy.
Principles of emergency management
Ketoacidotic coma:
- insulin and glucose replacement therapy;
- restoration of fluid volume, electrolytes and blood pH.
Hyperosmolar coma:
- restoration of fluid volume and osmotic blood pressure by administration of hypotonic (0.45%) sodium chloride solution (2-3 liters);
- administration of electrolytes with short-acting insulin preparations in small doses (5-10 U/hour).
Benefits of treatment at the clinic
- Doctors make a thorough diagnosis of diabetes and its complications in the body for treatment.
- We select an individual treatment program based on the latest clinical recommendations and the doctors' many years of clinical experience.
- Doctors give a detailed consultation to the patient about what recommendations and rules diabetics should follow.